Cdk5 controls lymphatic vessel development and function by phosphorylation of Foxc2

Nat Commun. 2015 Jun 1:6:7274. doi: 10.1038/ncomms8274.

Abstract

The lymphatic system maintains tissue fluid balance, and dysfunction of lymphatic vessels and valves causes human lymphedema syndromes. Yet, our knowledge of the molecular mechanisms underlying lymphatic vessel development is still limited. Here, we show that cyclin-dependent kinase 5 (Cdk5) is an essential regulator of lymphatic vessel development. Endothelial-specific Cdk5 knockdown causes congenital lymphatic dysfunction and lymphedema due to defective lymphatic vessel patterning and valve formation. We identify the transcription factor Foxc2 as a key substrate of Cdk5 in the lymphatic vasculature, mechanistically linking Cdk5 to lymphatic development and valve morphogenesis. Collectively, our findings show that Cdk5-Foxc2 interaction represents a critical regulator of lymphatic vessel development and the transcriptional network underlying lymphatic vascular remodeling.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cyclin-Dependent Kinase 5 / genetics*
  • Cyclin-Dependent Kinase 5 / metabolism
  • Endothelial Cells / cytology
  • Endothelial Cells / metabolism*
  • Forkhead Transcription Factors / genetics
  • Forkhead Transcription Factors / metabolism*
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Lymphangiogenesis / genetics*
  • Lymphatic Vessels / metabolism*
  • Lymphatic Vessels / pathology
  • Mice
  • Mice, Knockout
  • Phosphorylation
  • Real-Time Polymerase Chain Reaction
  • Stress, Mechanical

Substances

  • Forkhead Transcription Factors
  • mesenchyme fork head 1 protein
  • Cyclin-Dependent Kinase 5
  • CDK5 protein, human
  • Cdk5 protein, mouse